The nuclear receptor PXR is a lithocholic acid sensor that protects against liver toxicity
By J. Staudinger, B. Goodwin, Stacey A. Jones, D. Hawkins-Brown, K. I. MacKenzie, A. Latour, Yaping Liu, C. Klaassen, K. Brown, J. Reinhard and 3 more. Proceedings of the National Academy of Sciences of the United States of America, 2001
1,411 citations recorded by the source corpus.
Subfields: Endocrinology, Diabetes and Metabolism, Oncology, Pharmacology
View Paper: https://www.semanticscholar.org/paper/79f9937109d2531b93cf55143c34967353720386
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In Endocrinology, Diabetes and Metabolism
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Citations in the corpus
- Xenobiotic, Bile Acid, and Cholesterol Transporters: Function and Regulation (2010, background): “21) (Staudinger et al., 2001b, 2003; Cheng and Klaassen, 2006).”
- Bile Acid Signaling in Metabolic Disease and Drug Therapy (2014, background): “Mice treated with LCA or subjected to BDL showed induction of PXR target genes involved in bile acid detoxification, whereas pxr knockout mice were more susceptible to hepatotoxicity caused by LCA treatment or BDL, supporting the significance of the adaptive activation of PXR in the prevention of bi”
- Recent advances in 2D and 3D in vitro systems using primary hepatocytes, alternative hepatocyte sources and non-parenchymal liver cells and their use in investigating mechanisms of hepatotoxicity, cell signaling and ADME (2013, neutral): “Johns wort, it appears that PXR is also involved in the coordinate expression of transport proteins and of metabolizing enzymes responsible for bile acid homeostasis (Staudinger et al. 2001; Wang et al. 2012a).”